Effects of amyl nitrite on left ventricular relaxation in patients with borderline hypertension

Naggar, Charles Z.

doi:10.1016/0002-9149(82)90405-2

Cited by 3 publications

(2 citation statements)

References 23 publications

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“…Any of these mechanisms could well disturb the LV relaxation in the absence of an increase in LV wall thickness, as in many of the hypertensive subjects in this study. Signs of disturbed LV relaxation have also been reported 26 recently in borderline hypertensive subjects without LV hypertrophy.…”

Section: Discussionmentioning

confidence: 59%

Diastolic function of the heart in untreated primary hypertension.

Hartford¹,

Wikstrand²,

Wallentin³

et al. 1984

Hypertension

102

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SUMMARY To study left ventricular (LV) diastolic function of the heart in relation to blood pressure (BP) and other signs of hypertensive cardiac and peripheral vascular changes, isovolumic relaxation time and early diastolic filling were determined in four BP groups of untreated 49-year-old men: normotensive subjects (n = 20), men with borderline hypertension (n = 30), mild hypertension (n = 45), and moderate to severe hypertension (n = 24). Isovolumic relaxation time, measured as the distance between aortic closure (A 2 , phonocardiography) and mitral valve opening (echocardiography), and early diastolic filling, measured as the distance between mitral valve opening and the O point of the apexcardiogram, tended to increase with BP level, and the total interval from aortic closure to the O point (A 2 O interval) was significantly prolonged in the two groups with mild and moderate to severe hypertension. A prolonged A 2 O interval (>117% of expected value at observed heart rate) was seen in several hypertensives, who had no obvious increase in LV wall thickness on M mode echocardiography. This suggests that a prolonged LV relaxation time may be an early sign of cardiac involvement in primary hypertension. In the group with moderate to severe hypertension, an increase in LV wall thickness was seen together with an increase in resistance at maximal dilation in the calf. This supports the theory that when changes in cardiac structure develop they occur in parallel with structural changes also in the periphery. (Hypertension 6: 329-338, 1984) KEY WORDS • primary hypertension • left ventricular relaxation time • wall thickness • structural vascular changes I N recent years it has been recognized that disturbances in diastolic function of the heart are as important components of left ventricular (LV) dysfunction as an impaired inotropic state. Diastolic abnormalities of the LV have been demonstrated in ischemic heart disease, dilated and hypertrophic cardiomyopathies, and LV hypertrophy.1 " 7 The development of reliable indices of LV relaxation and filling allows us today to study noninvasively the diastolic function of the heart in asymptomatic patients. Such studies have revealed disturbances of LV relaxation and filling in patients with mild hypertension. This suggests that these diastolic abnormalities may be characteristic of early hypertensive heart disease. In the present study, the period of LV relaxation and early filling was determined in 119 middle-aged men and covered a wide blood pressure (BP) range to elucidate whether impairment of diastolic function is an early indicator of cardiac involvement in essential hypertension and to study the dependence of LV relaxation time on changes in LV wall thickness and some other pertinent variables. The investigation was further aimed at studying how cardiac structural changes are related to signs of increased resistance in peripheral vascular beds. Subjects and Methods Study PopulationWe recruited a study population of untreated men with BP varying from very low ...

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Section: Discussionmentioning

confidence: 59%

Diastolic function of the heart in untreated primary hypertension.

Hartford¹,

Wikstrand²,

Wallentin³

et al. 1984

Hypertension

102

View full text Add to dashboard Cite

show abstract

“…Any of these factors may be present in people with primary hypertension. The question also arises as to whether an impairment in the active energy-dependent intracellular shifts of calcium ions, that are necessary for relaxation to occur, could be of importance for a prolongation (Naggar, Stanley & Downing, 1982;Nayler & Williams, 1978). As discussed by Nayler and Williams, (1978) there are several possible ways for an impairment in active relaxation to be effected; for instance, an inadequate supply of ATP, a defective calcium-accumulating activity of the sarcoplasmic reticulum or an increased calcium influx from the extracellular space.…”

Section: Left Ventricular Wall Thickness and Left Ventricular Relaxationmentioning

confidence: 99%